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In this article, a uniform neural network (NN) digital predistortion (DPD) model of radio frequency (RF) power amplifiers (PAs) is proposed for dynamic applications, which is suitable for RF PAs under various operating conditions without updating the coefficients. With the development of communication systems, it is difficult for the DPD to track the nonlinearity of the PA as the operating condition varies frequently. As one of the most promising achievements in recent years, the NN has shown excellent generalization ability, which is applicable to the DPD for scalable applications. In this situation, a uniform neural network model (UNNM), whose structure is a two-stage network, is proposed for scalable output power, scalable bandwidth, or simultaneous scalable power and bandwidth. The experiments are carried out on two sub-6 GHz broadband GaN Doherty PAs (DPAs). The experimental results show that the proposed model can achieve comparable performance without coefficient update in the scalable output power range of about 5 dB and the bandwidth range of 100 MHz, which outperforms the conventional fixed model with better than 3 dB power range and 40 MHz bandwidth range. [ABSTRACT FROM AUTHOR]

The looseness of tires or even falling off from cars will lead to serious traffic accidents. Once it occurs, it will bring casualties and huge economic losses to society, seriously affecting the traffic safety. To mitigate such possible safety concerns, an early loosening warning system is developed in this article. The system consists of the tire monitoring module and the working control module. The tire monitoring module is installed on the tire and is designed with no power supply. The control module is installed in the vehicle body. Signal transmission between the two modules is achieved through wireless radio frequency. In the driving, once the tire is loosened, the monitoring device will send out the alarm signal automatically and wirelessly. After the driver gets the alarm signal, he can immediately perform the emergency processing, parking, and inspection, which can avoid traffic accidents caused by it. This article introduces the detailed structure, working principle, and operation process of the system. This early warning system has simple structure, high reliability, and is easy to use. It can be used in the common working environment of automobiles. Meanwhile, it is also the foundation of intelligent connected vehicle. [ABSTRACT FROM AUTHOR]

Background and Aims: Hepatic ischaemia/reperfusion injury (HIRI) is a pathophysiological process that occurs during the liver resection and transplantation. Reportedly, peroxisome proliferator‐activated receptor β/δ (PPARβ/δ) can ameliorate kidney and myocardial ischaemia/reperfusion injury. However, the effect of PPARβ/δ in HIRI remains unclear. Methods: Mouse hepatic ischaemia/reperfusion (I/R) models were constructed for in vivo study. Primary hepatocytes and Kupffer cells (KCs) isolated from mice and cell anoxia/reoxygenation (A/R) injury model were constructed for in vitro study. Liver injury and inflammation were investigated. Small molecular compounds (GW0742 and GSK0660) and adenoviruses were used to interfere with PPARβ/δ. Results: We found that PPARβ/δ expression was increased in the I/R and A/R models. Overexpression of PPARβ/δ in hepatocytes alleviated A/R‐induced cell apoptosis, while knockdown of PPARβ/δ in hepatocytes aggravated A/R injury. Activation of PPARβ/δ by GW0742 protected against I/R‐induced liver damage, inflammation and cell death, whereas inhibition of PPARβ/δ by GSK0660 had the opposite effects. Consistent results were obtained in mouse I/R models through the tail vein injection of adenovirus‐mediated PPARβ/δ overexpression or knockdown vectors. Furthermore, knockdown and overexpression of PPARβ/δ in KCs aggravated and ameliorated A/R‐induced hepatocyte injury, respectively. Gene ontology and gene set enrichment analysis showed that PPARβ/δ deletion was significantly enriched in the NF–κB pathway. PPARβ/δ inhibited the expression of p‐IKBα and p‐P65 and decreased NF–κB activity. Conclusions: PPARβ/δ exerts anti‐inflammatory and anti‐apoptotic effects on HIRI by inhibiting the NF–κB pathway, and hepatocytes and KCs may play a synergistic role in this phenomenon. Thus, PPARβ/δ is a potential therapeutic target for HIRI. [ABSTRACT FROM AUTHOR]

Targeting energy metabolism holds the potential to effectively treat a variety of malignant diseases, and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α) is a key regulator of energy metabolism. However, PGC1α′s role in cancer, especially in hepatocellular carcinoma (HCC) remains largely unknown. In the present study, we reported that PGC1α was significantly downregulated in HCC cell lines and specimens. Moreover, reduced expression of PGC1α in tumor cells was correlated with poor prognosis. PGC1α overexpression substantially inhibited cell proliferation and induced apoptosis in vitro and in vivo. On the contrary, the knockdown of PGC1α produced the opposite effect. The mechanism was at least partially due to the upregulation of mitochondrial pyruvate carrier 1 (MPC1) caused by PGC1α, which promoted mitochondrial biogenesis by binding to nuclear respiratory factor 1 (NRF1). Consequently, the production of cellular reactive oxygen species (ROS) caused by mitochondrial oxidation was elevated above a critical threshold for survival. Furthermore, we found that PGC1α could enhance the antitumor activity of sorafenib and doxorubicin in HCC through ROS accumulation-mediated cell death. These results indicate that PGC1α/NRF1-MPC1 axis is involved in HCC progression and could be a promising target for HCC treatment. Image 1 • Low expression of PGC1α and MPC1 was associated with the poor prognosis of HCC. • PGC1α and MPC1 could inhibit HCC cell proliferation and induce apoptosis. • PGC1α/NRF1-MPC1 axis activates mitochondrial biogenesis and drives ROS production. • PGC1α/NRF1-MPC1 axis attenuates HCC progression. • PGC1α could enhance the sensitivity to sorafenib/doxorubicin treatment in HCC. [ABSTRACT FROM AUTHOR]